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TRPC6 is a mechanosensitive channel essential for ultrasound neuromodulation in the mammalian brain

Yumi Matsushita, Kaede Yoshida, Miyuki Yoshiya, Takahiro Shimizu, Satoshi Tsukamoto, Nobuki Kudo, Yuichi Takeuchi, Makoto Higuchi, Masafumi Shimojo

Proceedings of the National Academy of Sciences 2024, 121 · 10.1073/pnas.2404877121

rodentin vitro cellhealthyinvasive electrophysiologycellular imaging

Abstract

Ultrasound neuromodulation has become an innovative technology that enables noninvasive intervention in mammalian brain circuits with high spatiotemporal precision. Despite the expanding utility of ultrasound neuromodulation in the neuroscience research field and clinical applications, the molecular and cellular mechanisms by which ultrasound impacts neural activity in the brain are still largely unknown. Here, we report that transient receptor potential canonical 6 (TRPC6), a mechanosensitive nonselective cation channel, is essential for ultrasound neuromodulation of mammalian neurons in vitro and in vivo. We first demonstrated that ultrasound irradiation elicited rapid and robust Ca 2+ transients mediated via extracellular Ca 2+ influx in cultured mouse cortical and hippocampal neurons. Ultrasound-induced neuronal responses were massively diminished by blocking either the generation of action potential or synaptic transmission. Importantly, both pharmacological inhibition and genetic deficiency of TRPC6 almost completely abolished neuronal responses to ultrasound. Furthermore, we found that intracerebroventricular administration of a TRPC6 blocker significantly attenuated the number of neuronal firings in the cerebral cortex evoked by transcranial ultrasound irradiation in mice. Our findings indicate that TRPC6 is an indispensable molecule of ultrasound neuromodulation in intact mammalian brains, providing fundamental understanding of biophysical molecular mechanisms of ultrasound neuromodulation as well as insight into its future feasibility in neuroscience and translational research in humans.

Abstract via europepmc.

Speciesmouse (C57BL/6J; TRPC6-KO)
Subjects3 animals
Sessions per subjectnot reported
Randomisednot reported
Blindingnot reported
Sham / controlinactive transducer
Auditory controldeafened subjects
Readout timingonline
Anaesthesiaanaesthetised
Readoutsinvasive electrophysiology, cellular imagingGCaMP6s fluorescence calcium imaging in cultured cortical/hippocampal neurons; in vivo extracellular multiunit recordings in cerebral cortex via tungsten microelectrode or 15-µm silicon probe; qPCR/RT-PCR for TRPC6 expression
Direction of effectexcitatoryUltrasound irradiation induced rapid Ca2+ transients in cultured neurons and intensity-dependent increases in population neural activity in mouse cerebral cortex; both effects required the mechanosensitive channel TRPC6 and were greatly reduced by TRPC6 blockade or knockout.
Adverse eventsnot reported

Exposures

Exposure 1: Cultured cortical/hippocampal neurons (in vitro Ca2+ imaging)

Target: cultured neurons — “cultured mouse cortical and hippocampal neurons
Device: other named manufacturer · NEPA GENE · ST-TM1-6 transducer with SonoPore KTAC-4000 amplifier

Pulse timing
Waveformpulsed
Fundamental frequency (kHz)1,000✓✓
Pulse duration (ms)5✓✓
Pulse repetition frequency (Hz)100✓✓
Duty cycle (%)50pulse duration × PRF gives 50%✓✓
Sonication duration (s)0.1, 0.2, 0.5swept?
Pressure and intensity, by domain
Free-field pressure (kPa)not reported
Free-field Isppa (W/cm²)0.38✓✓
Free-field Ispta (W/cm²)0.017, 0.19, 0.294swept?
In-situ estimatenot applicable
In-situ pressure (kPa)not applicable
In-situ Isppa (W/cm²)not applicable
In-situ Ispta (W/cm²)not applicable
Protocol, in the paper’s words

Neurons were stimulated with ultrasound waves at a frequency of 1 MHz. Each stimulus consisted of 100 Hz PRF with a duty cycle of 50%. Neurons were sonicated at different stimulation parameters in terms of irradiation intensities (17, 190, 294 mW/cm2) and durations (100, 200, 500 msec); an intensity of 190 mW/cm2 and a duration of 500 msec were chosen for all subsequent experiments.

Exposure 2: Transcranial ultrasound to cerebral cortex (in vivo electrophysiology)

Target: cerebral cortex — “cerebral cortex (2.06 mm posterior, 0.36 mm rightward from bregma)
Device: other named manufacturer · NEPA GENE · ST-T1-3 transducer with SonoPore KTAC-4000 amplifier

Pulse timing
Waveformpulsed
Fundamental frequency (kHz)1,000✓✓
Pulse duration (ms)5✓✓
Pulse repetition frequency (Hz)100✓✓
Duty cycle (%)50pulse duration × PRF gives 50%✓✓
Sonication duration (s)0.1✓✓
Pressure and intensity, by domain
Free-field pressure (kPa)160✓✓
Free-field Isppa (W/cm²)not reported
Free-field Ispta (W/cm²)0.07, 0.13, 0.21, 0.35, 0.52, 0.73swept✓✓
In-situ estimatenot reported
In-situ pressure (kPa)not reported
In-situ Isppa (W/cm²)not reported
In-situ Ispta (W/cm²)not reported
Protocol, in the paper’s words

Transcranial ultrasound irradiation of 1 MHz in 100 Hz PRF and 50% duty cycle, the same parameter as in our in vitro experiments. Basic parameters of the ultrasound burst pulse sequence are the same as that used for in vitro studies, but the train contains 10 burst pulses, and the duration is 100 msec. At each recording site, several recording sessions at different ultrasound intensities (0, 70, 130, 210, 350, 520, 730 mW/cm2) were performed; ultrasound stimulations were performed 20 times with a random interstimulus interval ranging from 10 to 20 s.

Flags from extraction

  • model_systemStudy combines an in vitro cultured-neuron mechanism experiment with an in vivo transcranial mouse experiment; n_subjects and subject_unit reflect only the in vivo animal experiment (3 mice).
  • n_sessions_per_subjectPaper reports 73 pre- and 80 post-drug recording sessions pooled across three mice, without stating sessions per individual mouse.
  • exposures[0].free_field.ispta_w_cm2Three intensities (17, 190, 294 mW/cm2) were tested as a sweep; only the 190 mW/cm2 condition was independently confirmed to match the calculated ISPTA (0.19 W/cm2).
  • sham_typeThe 0 mW/cm2 condition in the in vivo intensity sweep is treated as the inactive/no-output control condition; no separate device-off sham session is described.